Samantha Butler received her B.A. in Natural Sciences from Cambridge University in 1990. For her Part II project in Genetics, she worked in Michael Akam’s laboratory characterizing novel mutations in the homeotic gene, Ultrabithorax in Drosophila melanogaster. She joined Yash Hiromi’s laboratory in 1990 at Princeton University for her Ph.D., studying the genetic mechanisms that establish cell fate in the Drosophila eye. She moved to vertebrates for her postdoctoral fellowship in 1997, joining Jane Dodd’s laboratory at Columbia University to examine neural circuit formation in the developing spinal cord. During this time, she was the first to identify the key role that inductive growth factors can play as axon guidance factors, showing that the bone morphogenetic proteins (BMPs) act as a repellent from the roof plate, directing commissural axons ventrally.
Dr. Butler started her own laboratory in 2004, where she has been exploring how the developmental mechanisms that first establish the neural tube can be reused to regenerate damaged or diseased spinal circuitry. Her laboratory has continued to dissect the mechanisms by which BMPs direct cell fate and axon guidance decisions. Recent findings include showing that BMPs do not act as morphogens to pattern the spinal cord as previously thought; rather, each BMP ligand promotes either progenitor patterning and/or neuronal differentiation to direct a unique range of sensory relay neurons. Dr. Butler has leveraged this understanding to establish the first directed differentiation protocols to derive spinal sensory neurons from mouse and human stem cells. Dr. Butler has also identified a critical mechanism by which the rate of axon outgrowth is controlled during embryogenesis, thereby permitting neural circuits to develop in synchrony with the rest of the embryo. Most recently, her studies have reignited the debate about the mechanism by which netrin1, the first axon guidance cue to be identified in vertebrates, functions in the spinal cord. Work from her laboratory has demonstrated that netrin1 promotes ventrally-directed axon growth not by chemotaxis, but rather by haptotaxis, the directed growth of cells along an adhesive surface. These studies have also suggested that neural progenitors have an intrinsic capacity to form axon growth tracts, an insight might be critical for promoting directed, fasciculated regenerative axonal growth.
Previous Chairs Include: